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Review
. 2013 May 12:2013:191823.
doi: 10.1155/2013/191823.

Atherosclerosis, dyslipidemia, and inflammation: the significant role of polyunsaturated Fatty acids

Mariarita Dessì  1 , Annalisa Noce, Pierfrancesco Bertucci, Simone Manca di Villahermosa, Rossella Zenobi, Veronica Castagnola, Eliana Addessi, Nicola Di Daniele
Affiliations
Review

Atherosclerosis, dyslipidemia, and inflammation: the significant role of polyunsaturated Fatty acids

Mariarita Dessì et al. ISRN Inflamm. .

Abstract

Phospholipids play an essential role in cell membrane structure and function. The length and number of double bonds of fatty acids in membrane phospholipids are main determinants of fluidity, transport systems, activity of membrane-bound enzymes, and susceptibility to lipid peroxidation. The fatty acid profile of serum lipids, especially the phospholipids, reflects the fatty acid composition of cell membranes. Moreover, long-chain n-3 polyunsatured fatty acids decrease very-low-density lipoprotein assembly and secretion reducing triacylglycerol production. N-6 and n-3 polyunsatured fatty acids are the precursors of signalling molecules, termed "eicosanoids," which play an important role in the regulation of inflammation. Eicosanoids derived from n-6 polyunsatured fatty acids have proinflammatory actions, while eicosanoids derived from n-3 polyunsatured fatty acids have anti-inflammatory ones. Previous studies showed that inflammation contributes to both the onset and progression of atherosclerosis: actually, atherosclerosis is predominantly a chronic low-grade inflammatory disease of the vessel wall. Several studies suggested the relationship between long-chain n-3 polyunsaturated fatty acids and inflammation, showing that fatty acids may decrease endothelial activation and affect eicosanoid metabolism.

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Figures

Figure 1
Figure 1
Effects of unbalanced n-6:n-3 dietary fatty acid intake on inflammatory state. EPA: eicosapentaenoic acid; DHA: docasahexaenoic acid; AA: arachidonic acid; PPAR-α: peroxisome proliferation-activated receptors-α; TX A2: thromboxane A2; TX  A3: thromboxane A3; NF-κB: nuclear factor kappa light-chain enhancer of activated B cells; PGE2: prostaglandin E2; PGE3: prostaglandin E3; LTB: leukotriene; SREBP-1c: sterol regulatory binding protein 1c.
Figure 2
Figure 2
Relationship between inflammation, atherosclerosis, and n-3-PUFA. NF-κB: nuclear factor kappa light-chain enhancer of activated B cells; ROS: reactive oxygen species; cPLA2: cytosolic phospholipase A2; COX-2: cyclooxygenase-2; i-NOS: inducible nitric oxide synthase; VCAM-1: vascular cell adhesion protein 1; ICAM-1: intercellular adhesion molecule-1; IL-8: interlukin-8; MCP-1: monocyte chemoattractant protein-1; TF: tissue factor; ET-1: endothelin-1; TX A2: thromboxane A2.
Figure 3
Figure 3
Factors and cells involved in the development of atherosclerosis. ROS: reactive oxygen species; LPO-products: lipo-peroxidation products; NF-κB: nuclear factor kappa light-chain enhancer of activated B cells.
See this image and copyright information in PMC

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